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Nephrol Dial Transplant (2000) 15: 1293–1297 Renal disease in Australian Aborigines
Menzies School of Health Research, Darwin, Northern Territory, Australia Introduction
We have been studying renal disease in the Tiwi Island Aboriginal people (population about 1800)since 1990. Their annual incidence of treated ESRD In this era of increasing accountability in population- incidence peaked at 2706 per million between 1993 and based research, and demands for strong evidence base 1996 [2], and their recent cardiovascular death rates of clinical practice, we need to examine justifications were 6-times those of an age-matched affluent non- for the study of catastrophic problems in indigenous Aboriginal population in Canberra, Australia’s capital or transitional people. One justification might be the [4]. In this study, more than 80% of the adult popula- illumination of risk factors for, and mechanisms of, tion, have been screened for renal disease, using the disease that can be generalized to the broader albumin/creatinine ratio (ACR, g/mol ) on a random population, where they might be obscured by lower urine specimen as the marker, and the natural history disease rates and density of risk factors. A more has been followed on many for 1–8 years (mean important justification is to arrive at, and model, solutions. We report a programme which has happilydone both.
Australian Aborigines are a disenfranchized and marginalized people in a crisis of epidemiologic trans-ition. Most Aborigines in the Northern Territory of Rates and associations of renal disease
Australia live in remote areas, in serious poverty anddisadvantage, with inadequate services of all types.
On cross-sectional examination of the community pro- Standardized adult mortality rates are more than four file [6 ], there was a relentless increase in ACR with times that of non-Aboriginal Australians, with all increasing age (Figure 2). Pathologic albuminuria was major conditions, including cardiovascular disease, pervasive in adults (20+ years); 23% had microalbumi- represented in excess [1]. Premature death in young nuria, (ACR 3.4–33) and 30% had overt albuminuria and middle age adults is contributing to family, (ACR 34+). There was a progressive decrease in GFR with increasing ACR starting in the early-mid micro- Renal disease and renal failure marks this ‘force of albuminuria range (Figure 3). Factors that correlated mortality’. Renal deaths are increased 18- to 30-fold, significantly with ACR included increasing age, birth while the incidence of treated end-stage renal disease weight and infant weight at one year (inversely), adult ( ESRD) is approaching 1000 per million, and doubling weight gain with central fat deposition and the accom- every 3–4 years, as shown in Figure 1 [2]. Increased panying features of Syndrome X (increasing blood ascertainment and referral probably contributed to this pressure, levels of insulin, blood glucose, lipids, and increase over the 1980s, but later increases have been diabetes). They also included skin sores, scabies and a real. Renal disease has attracted especial concern because of the cost of treating people with ESRD, (PSGN ), heavy drinking, multiparity in women (3 or with an annualized cost per patient on haemodialysis more children), and a family history of renal disease.
(the main form of treatment) recently estimated at The estimated risk enhancement for overt albuminuria $100 000 [3]. In 1998, 96% of people on dialysis in the associated with these ‘diagnoses’ was substantial [5,6 ].
Northern Territory were Aboriginal, although they We thus proposed a multideterminant model of renal constitute only 28% of the population. The costs are disease in which the simultaneous operation of enormous, quality of life is poor, and survival, several risk factors progressively enhances the increase reflecting the generally poor health of Aboriginal in albuminuria that accompanies increasing age.
Multivariate models predict a fairly low prevalence ofrenal disease in people with no risk factors, but almostinevitable presence of overt albuminuria by middle life Correspondence and offprint requests to: Dr Wendy Hoy, Menzies in people with a full menu of risk factors [5]. In such School of Health Research, PO Box 41096, Casuarina, NT 0811,Australia.
a model, nephropathic factors would potentiate renal 2000 European Renal Association–European Dialysis and Transplant Association Fig. 1. Average annual ESRD incidence (cases per million) in Aboriginal people in the top end of the Northern Territory.
Fig. 2. ACR, g/mol, by age group.
Fig. 3. Correlation between ACR and GFR on baseline screen*
(adjusted for age, sex and BMI ).
disease expression and progression rather than act as‘single cause’ agents.
Natural history of renal disease
ACR increased and GFR fell in individuals with time,at rates that were strongly correlated with the severityof baseline disease [7]. In people with ACR 34+ atbaseline, the average fall in GFR was 4.1 ml/min/year.
All renal failure arose in people who had heavy albu-minuria at baseline, as shown in Figure 4 [7,8]. Therewas also a strong correlation between baseline ACRand subsequent natural death ( Figure 4), whichincluded, but were not restricted to, cardiovasculardeaths [8,9]. After accounting for age and sex, thehazard ratio of persons with microalbuminuria fornatural death compared with those of lower ACRswas 2.3 (95% CI 1.0–5.3), for those with ACR 34–99 Fig. 4. Natural deaths and ESRD by baseline ACR category.
was 3.2 (1.3–7.9), and for those with overt albumin- the D allele of the angiotensin converting enzyme gene uria was 5.1 (2.1–12.8). The estimated 5 year mortality is underrepresented in this and other Aboriginal (nonrenal and renal ) in people with ACR 34+ at groups, so while it may enhance disease progression in baseline was 35%. Thus ACR in this population marks the few people so endowed, this allele is not the major not only renal disease and risk of ESRD, but also driving element in renal disease expression [16 ].
cardiovascular risk and the general force of mortality.
Health services and disease expression
Renal size and renal morphology
Health services and other services also influence renal Our studies suggest that reduced nephron endowment disease expression. Some initiatives should reduce dis- or impaired nephron maturation might predispose to ease rates (environmental hygiene, vaccines, improved renal disease. This might be a consequence, in part, of nutrition etc), and medicines may reduce disease pro- intrauterine growth retardation and infant malnutri- gression, as described later. However, improved ser- tion, as we have shown a clear relationship of body- vices are also, ironically, enhancing disease expression.
surface-area adjusted kidney volume to birth weight Dramatic recent reductions in infant mortality between by ultrasound study of children in this community [9].
the 1960s and 1980s have allowed large cohorts of low In view of the 4-fold difference in nephron number birth weight persons to survive to adult life at high described in the general population [10], lower renal risk for chronic disease [6 ]. In addition, prolongation volume might also have a genetic component. This is of life due to better management of infections and likely to be adaptive; a smaller number of nephrons diabetes, and postponement of cardiovascular deaths might have been entirely adequate in the previous by patchy antihypertensive treatment, coronary angi- subsistence state, or even a survival advantage in oplasties, bypass grafting etc, are now allowing the conditions of salt and water deprivation.
more leisurely development of nephropathy to run its Findings in ‘diseased’ renal biopsies in this commun- full course in a larger proportion of people.
ity and other NT Aboriginal people are compatiblewith these hypotheses. All the usual morphologic dia-gnoses are represented to some degree, which supportsthe multideterminant hypothesis, and many biopsies Pharmacologic renal and cardiovascular protection
show nonspecific change [11]. The striking consistentfindings are glomerulomegaly and various degrees of In November 1995 we introduced a systematic treat- glomerular sclerosis, with which glomerular size is ment programme for people in this community with strongly correlated [12,13]. This glomerulomegaly pathologic albuminuria or hypertension. The primary probably represents excessive nephron hypertrophy.
treatment agent was the long acting angiotensin con- Nephron hypertrophy is the mechanism by which all verting enzyme, perindopril (Coversyl, Servier). Target kidneys enlarge until adulthood, and might be exacer- blood pressure was <130/80 mmHg at first, and more bated by the trophic effects of the Syndrome X state recently <120/75 mmHg [17,18]. By December 1998, in adolescence and adult life. This trophie stimulus 240 people had enrolled, 46% were diabetic, 64% would be further magnified if the number of existing hypertensive and 67% had overt albuminuria and 12% nephrons were already reduced, due to compromised had elevated serum creatinine at the start of treatment.
nephron endowment in utero [14], or destruction of Participation has been enthusiastic, and compliance nephrons by nephropathic factors during postnatal has been good in 67%. Blood pressure responses have life. Hyperperfusion associated with nephron hyper- been dramatic, and albuminuria and GFR have stabil- trophy provides a theoretical mechanism for increasing ized on a group basis. By December 1998, with a mean albuminuria and accelerated nephron loss in this state.
time on treatment of 2.1 years, there had been aestimated 55% reduction in new cases of ESRD and a45% reduction in natural deaths in the ‘intention to Family clustering of renal disease
treat’ group compared with historical controls matchedfor disease severity. Maximum benefit (62% reduction) A recent study from our group has shown a correlation accrued in people with overt albuminuria, in whom between socioeconomic disadvantage and ESRD rates most of these events were segregated, as shown in among Aboriginal people that was so powerful, given Figure 5. Reductions in community-based rates of the serious poverty of people in most high risk areas, ESRD and natural deaths support these estimates there might be little need to propose an additional ( Figure 6). We estimate savings on dialysis costs alone major intrinsic predisposition [15]. However, it is clear in this small community (est 1800 people) between that renal disease is more frequent and more severe in $700 000 Aust and $3.1 million, in the first 3 years, some families than others. We are attempting to ascer- depending on whether ESRD and death rates would tain the relative contributions of environment and have continued to escalate or would have achieved a genotype to this phenomenon, with studies of family plateau in the absence of the programme [2,3,18]. The clustering of phenotypic and clinical features, as well reduction in sickness and death is, however, a more as potential susceptibility genes. We already know that expensive and achieves no net gain in population-based health.
Many of these findings might be generalized to other high risk populations. The medical community shouldadvocate for intersectoral initiatives to improve generalliving standards, where needed, and foster inter-specialty collaborations for a unified approach tohealth issues, based on community-based prevention,screening and treatment programs. We must directsubstantial intellectual and material resources to theseissues and reposition medical and specialist trainingcurricula to reflect those views. Constant evaluation ofthe outcomes of such community-based programmesis essential to modify strategies appropriately. Withthese approaches, better health, reduced deaths andlower health care costs can probably be achieved overa shorter term than ever imagined.
Fig. 5. Renal failure and natural deaths, historical controls vs
‘Intention to treat’.
Acknowledgements. This review is derived from an ambitious projectthat began in 1989, instigated through the perspectives and initiativesof Professor John Mathews, Dr David Pugsley, and Paul VanBuynder. Zhiqiang Wang, Philip Baker, Janine Spencer, BeverlyHayhurst, Desire´e Silva, Emma Kile, Megan Rees, Kate Walker,Angela Kelly, Kiernan McKendry and Susan Jacups have all ledvarious elements of the field work and basic inverstigation. Wethank the laboratory and Renal Unit staff at Menzies, the laboratorystaff at the Royal Darwin Hospital, and all our multidisciplinarycollaborators for their efforts. We especially thank the Tiwi peoplewho have participated eagerly in the community-based elements ofthis program, and their Land Council and Health Board for theirsupport and oversight. The work of health workers Colleen Kantilla,Darren Fernando, Jerome Kerinaiuia and Nellie Punguatji, andCommunity Project Officers, Elizabeth Tipiloura and Eric Tipilourahas, has been invaluable. The program has been supported by fundsfrom the National Health and Medical Research Council, the StanleyTipiloura fund, the Australian Kidney Foundation, Rio Tinto,Servier, Australia, Janssen Cilag and Territory Health Services, andthe New Children’s Hospital in Sydney, Australia.
Fig. 6. New cases of ESRD and natural deaths in Tiwi adults
(20+ years).
1. Cunningham J, Condon J. Premature mortality in Aboriginal Conclusions
adults in the Northern Territory. Med J Aust 1996; 165: 309–312 2. Spencer JS, Silva D, Hoy WE. An epidemic of renal failure among Australian Aborigines. Med J Aust 1998; 168: 537–541 Renal disease is pervasive in this population and 3. You J, Hoy W, Beaver C, Zhao Y. Costs of hemodialysis and progresses over time. It is multideterminant, educed hospitalisations for patients with end stage renal disease in theTop End of the Northern Territory. The 35th Annual Scientific by a number of factors operating in a high risk Meeting of the Aust NZ Soc Nephrol, 3–5 March, 1999 environment, and intimately related to the general 4. Jain SK (ed ). Trends in mortality by causes of death in Australia, health profile [22]. Risk factors derive from, or are the states and territories during 1971–1992, and in statistical exacerbated by, rapid epidemiologic transition, serious subdivisions during 1991–1992. ABS catalogue no 3313.0, poverty and disadvantage, and the deficiencies and National Centre for Epidemiology and Population Health andAustralian Bureau of Statistics, 1994 successes of health services. Environmental factors 5. Hoy WE et al. The multidimensional nature of renal disease: have probably also influenced genotypes over time.
rates and associations of albuminuria in an Australian Prevention depends on sustained improvements in Aboriginal community. Kidney Int 1998; 54: 1296–1304 6. Hoy WE, Kile E, Rees M, Mathews JD. A new dimension to the Barker hypothesis: low birth weight predisposes to albumin- health services. For persons already afflicted, disease is uria: findings in an Australian Aboriginal community. Kidney easily diagnosed and progression is dramatically altered by standard interventions within our reach 7. Hoy WE, Van Buynder P, Hayhurst B et al. The natural history [20]. Control of blood pressure, adult weight and of renal disease in an Australian Aboriginal community. The infections are especially important. Pharmacologic 35th Annual Scientific Meeting of the Aust NZ Soc Nephrol,3–5 March, 1999 treatment reduces premature death in early and mid 8. McDonald S, Wang Z, Hoy WE. Physical and biochemical adult life and might postpone renal failure beyond predictors of death in an Australian Aboriginal cohort. Clin reasonable life expectancies in many people. The Exp Pharmacol Physiol 1999; 26: 618–621 expansion of ESRD treatment services is enormously 9. Spencer J, Wang Z, Hoy WE. Is low birth weight linked to renal disease through impaired nephrogenesis? Birth weight and renal 16. McDonald S, Panagiotopoulos S, Smith T, Hoy W, Mathews volume in Aboriginal children. The 35th Annual Scientific JD. Angiotensin converting enzyme (ACE ) polymorphisms and Meeting of the Aust NZ Soc Nephrol, 3–5 March, 1999 renal disease in Aboriginal Australians. The 36th Annual 10. Nyengaard JR, Bendtsen TF. Glomerular number and size in Scientific Meeting of the Aust NZ Soc Nephrol, 13–15 March, relation to age, kidney weight, and body surface in normal man.
Anatomical Record 1992; 232: 194–201 17. Hoy WE, Baker P, Kelly A et al. Stemming the tide: Reducing 11. Lloyd ML, Moore L, Pugsley DJ, Seymour AM. Renal disease cardiovascular disease and renal failure in Australian Aborigines.
in an Australian Aboriginal population: a pathologic study.
18. Hoy WE, Baker P, Kelly A, Wang Z. No more excuses. Reducing 12. Bertram JF, Young RJ, Kincaid Smith P, Seymour AE, Hoy premature death and renal failure in Australian Aborigines. Med WE. Glomerulomegaly in Australian Aborigines. Nephrology 4 19. Baker P, Hoy WE, Wang Z et al. Towards evaluation of the 13. Young RJ, Kincaid Smith P, Hoy WE, Bertram JF. Glomerular cost-effectiveness of a treatment program for renal disease in size and glomerulosclerosis in Australian Aborigines. Am Australian Aborigines. The 35th Annual Scientific Meeting of the Aust NZ Soc Nephrol, 3–5 March, 1999 14. Lucas SRR, Costa Silva VL, Miraglia SM, Gil FZ. Functional 20. Hoy WE. Renal disease as metaphor: towards a more integrated and morphometric evaluation of offspring kidney after intra- view of Aboriginal health. The Austin Doyle Lecture: High uterine undernutrition. Pediatric Nephrol 1997; 11: 719–723 15. Cass A, Cunningham J, Wang Z, Hoy W. End stage renal Blood Pressure Council of Australia. Clin Exp Pharmacol Physiol disease ( ESRD) in indigenous Australians: a disease of poverty.
The 36th Annual Scientific Meeting of the Aust NZ Soc Nephrol, 21. Hoy WE. Screening and treatment for renal disease: the 13–15 March, 2000, Melbourne, Australia community model. Nephrology 1998; 4 [Suppl iiı–iv]: S90–95

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